PAIN Flashcards

1
Q

What is pain?

A
  • an unpleasant sensory & emotional experience
  • a/w actual/potential tissue damage
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2
Q

Classification of pain? (duration & pathophysiology)

A

Duration
- acute
- chronic
- breakthrough

Pathophysiology
- nociceptive (split into somatic & visceral)
- neuropathic

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3
Q

Diff between acute and chronic pain? (in terms of onset)

A

Acute: recent onset & probable limited duration

Chronic: last >3-6m or persists beyond duration of an acute disease, or after tissue healing is complete

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4
Q

Diff between acute and chronic pain? (in terms of type of pain)

A

Acute: nociceptive usually, but can be neuropathic

Chronic: nociceptive, neuropathic or both

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5
Q

Diff between acute and chronic pain? (in terms of sx)

A

Acute: sharp, dull, shock-like, tingling, shooting, radiating, fluctuating in intensity, varying in location (timely r/s with obvious noxious stimuli)

Chronic: same as acute but no timely r/s, pain stimulus may cause sx that completely change (e.g. sharp to dull)

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6
Q

Diff between acute and chronic pain? (in terms of signs)

A

Acute: can cause HTN, tachycardia, diaphoresis, mydriasis, pallor

Chronic: comorbid conditions often present, whatever listed in acute is seldom present

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7
Q

Diff between the cause of neuropathic and nociceptive pain?

A

Neuropathic: caused by lesion / disease of somatosensory nervous system

Nociceptive: arises from actual / threatened damage to non-neural tissue, due to activation of nociceptors in an individual with a normally functioning somatosensory nervous system

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8
Q

Features of neuropathic, somatic & visceral pain?

Where somatic & visceral pain arise from, characteristics of each pain

A

Neuropathic: burning, sharp stabbing pain, like electric shock (hyperalgesia or allodynia)

Somatic: arise from damage to body tissues, sharp / hot / stinging, localised

Visceral: arise from viscera mediated by stretch receptors (from internal organs), usually accompanied by N/V

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9
Q

What is hyperalgesia and allodynia?

A

Hyperalgesia: exaggerated painful responses to normally noxious stimuli

Allodynia: painful responses to normally non-noxious stimuli

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10
Q

What is SOCRATES used for and what does it stand for?

A

Used for pain hx taking

Site
Onset
Characteristics
Radiation
Associated sx
Time course
Exacerbating / relieving factors
Severity

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11
Q

What are the pain scores used to assess pain?

A
  • numeric rating scale
  • verbal descriptor scale
  • faces pain scale
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12
Q

What is the pain ladder from WHO?

A
  1. non-opioid +- adjunvant
  2. opioid for mild-moderate pain +- non-opioid +- adjuvant
  3. opioid for moderate-severe pain +- non-opioid +- adjuvant
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13
Q

What are non-opioids?

A

Paracetamol, NSAIDs

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14
Q

What are weak and strong opioids?

A

Weak: tramadol, codeine etc
Strong: morphine, fentanyl etc

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15
Q

When is paracetamol absolutely CI and cautioned in?

A

CI: Liver failure
Caution: hepatic insufficiency, chronic alcohol abuse or dependence

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16
Q

When is NSAIDs CI?

A
  • GI ulcer/bleed
  • asthma
  • pregnancy 3rd trimester
  • kidney problem
  • CVD (uncontrolled HTN, HF, IHD)
  • allergy
  • liver problem
  • bleeding disorder / meds
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17
Q

What are the greatest risk a/w COX-1 and COX-2 inhibition activity?

A

COX-1: upper GI bleed/perforation
COX-2: CVD

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18
Q

Do NSAIDs help with non-specific low back pain?

A

No

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19
Q

Is celecoxib or etoricoxib more COX-2 selective?

A

Etoricoxib

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20
Q

Selectivity from COX-1 to COX-2? (12 drugs)

A

Ketoprofen, piroxicam, indometacin, aspirin, naproxen, ibuprofen, diclofenac, mefenamic acid, meloxicam, celecoxib, parecoxib, etoricoxib

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21
Q

NSAIDs MOA?

A

Block COX (which breaks down AA to prostaglandins TXA2, PGE2, PGI2)

22
Q

Function of PGI2, PGE2 and TXA2?

A

PGI2: vasodilation, inhibit platelet aggregation
PGE2: vasodilation, vasoconstriction, vascular permeability (swelling), pain
TXA2: vasoconstriction, platelet aggregation

23
Q

MOA of codeine?

A

weak mu & delta opioid agonist -> metabolised to morphine by CYP2D6

24
Q

MOA of tramadol?

A

weak mu opioid agonist & inhibit reuptake of NA & serotonin

25
Q

When should dose of tramadol be reduced?

A

≥75y, hepatic+/ renal impairment (lower seizure threshold)

26
Q

Is morphine more or less constipating than fentanyl?

A

More constipating

27
Q

What is the active metabolite of morphine? What happens in renal impairment?

A

Morphine-6-glucuronide, accumulates and cause more SE

28
Q

How often should fentanyl patch be changed? How long does fentanyl stay effective after removal of the patch? Does fentanyl patch work immediately?

A

Q72h

Stays effective for up to 12h after removal

Does not work immediately, takes 10-18h

29
Q

Lowest dose of fentanyl patch? Can the patch be cut to give the lower dose?

A

6mcg/hr (half of 12mcg patch)

Cannot cut patch, peel off half of the backing and paste on skin

30
Q

Common SE of opioids? (9)

A

Constipation, drowsiness, N/V, dry mouth, urinary retention, delirium, itch/rash, hyperalgesia, resp depression

31
Q

To prevent opioid-induced constipation, what should the pt be given?

A

2 REGULAR laxatives (Senna, lactulose)

32
Q

Conversion between diff opioids?
- codeine:morphine
- tramadol:morphine
- oxycodone:morphine
- fentanyl:morphine
- morphine SC:morphine PO
- fentanyl PO: fentanyl TD

A
  • codeine:morphine = 10:1
  • tramadol:morphine = 5:1
  • oxycodone:morphine = 2:1
  • fentanyl:morphine = 100:1
  • morphine SC:morphine PO = 3:1
  • fentanyl PO: fentanyl TD = 1:1
33
Q

What units is fentanyl patch?

A

mcg

34
Q

If pain was effectively controlled and pt is opioid tolerant, what should be done to the dose after conversion? Why?

A

Reduce dose by 25-50% to allow for incomplete cross tolerance b/w opioids

35
Q

If previous dose was ineffective, what should be done to the dose?

A

Keep at 100% or up to 125% of prev dose

36
Q

What can be used for neuropathic pain?

A

Gabapentin, pregabalin, amitriptyline, nortriptyline, topical lidocaine

37
Q

What kind of pain can corticosteroids be used for?

A
  • bone pain
  • neuropathic pain
  • raised intracranial pressure
  • liver capsule stretch pain
38
Q

What can be used for bone pain?

A

Bisphosphonates

39
Q

What can be used for cramps / muscle spasm?

A

Muscle relaxants (e.g. baclofen), benzodiazepines

40
Q

What can be used for intestinal colic?

A

Hyoscine butylbromide

41
Q

Can aspirin be used in <16y? Why?

A

No, due to risk of Reyes syndrome

42
Q

Which NSAID has a lower risk of cardiovascular toxicity than the rest?

A

Naproxen

43
Q

What is the difference between naproxen sodium and naproxen base?

A

Naproxen sodium has more rapid absorption & onset of effect than naproxen base

44
Q

Up to how often can topical pain preparations be applied? Any exceptions?

A

up to QDS

EXCEPT ketoprofen & diclofenac patch (only 2 patches in 24h)

45
Q

1st lines for neuropathic pain?

A
  • amitriptyline
  • duloxetine
  • gabapentin
  • pregabalin
46
Q

What is topical capsaicin used for?

A

Neuropathic pain

47
Q

1st line for trigeminal neuralgia? Other possible treatments?

A

1st line: Carbamazepine

Others: lamotrigine, gabapentin, pregabalin

48
Q

When can tramadol be used for neuropathic pain?

A

If acute rescue therapy is needed

49
Q

Can gabapentin/pregabalin be used in pregnancy?

A

Not recommended

50
Q

Nonpharm for pain?

A
  • exercise, posture
  • superficial heat
  • cryotherapy
  • transcutaneous electrical nerve stimulation (TENS)
  • massage
51
Q

How do NSAIDs cause AKI?

A
  • inhibit PGE2: increase Na & water retention -> peripheral edema, HTN
  • inhibit PGI2: suppress RAAS -> less K excretion -> hyperK
  • vasoconstriction of afferent arteriole -> reduce renal perfusion
52
Q

NSAIDs SE?

A
  • GI ADR (dyspepsia, N/V, anorexia, abd pain, ulcers)
  • renal ADR (AKI)
  • pseudo-allergic reaction (excess leukotrienes from inhibiting COX)
  • asthma (excess leukotrienes from inhibiting COX)
  • bleeding
  • reproduction ADR (CI in 3rd trimester of pregnancy due to premature closure of ductus arteriosus)
  • wound healing impairment
  • thrombosis
  • heart attack & stroke